Aroa Mañas-Ojeda

I have a lot of respect for Dr. Barbacid. But he is not even close to curing cancer. He worked on KRAS in mice and I worked on KRAS in human ... so I understand what he did and the relevance but also the complexity. KRAS mutations is one way to develop cancer. There are mutations in TP53, CDKN2A/p16, and SMAD4/DPC4, along with DNA damage repair genes like BRCA1/2 and ATM. Alternative drivers BRAF, ALK, NRG1, RET, and ROS1, ERBB2 and more. They cause cancer too. That means cancer can manifest in many ways and cancer cannot be treated with one treatment option. We also have similar treatment in clinical trials for KRAS. Also translation from mouse to human is a huge issue with this study ... He used mice and mice are more resilient to cancer - Most mice in labs get cancer because we inject stuff into it to induce cancer or because they are transgenics. They do not naturally get cancer (most of the time). This is different to humans. There are differences between induced tumors and naturally formed tumors and how they respond to treatment. Mice live for 2 years and humans on average over 70 years. The tumor has more time to cook inside a human creating more complexity. For example what I encountered in human studies is a phenomenon called cancer heterogeneity. One mutation creates other mutations. So even within the same person there can be two tumors that has different mutation complexities. But this takes time. Mice do not live long enough to experience this. So ... here is my estimation for the study based on complexities surrounding this research. He needs to first validate efficacy and toxicity (usually human cell lines, organoids, cats and dog studies where ethics really slow down things and make all studies more expensive) Once that has been validated this can be taken into a small human trial ... first to see if it works ... and then later to see toxicity and efficacy etc. Then if all that works ... three phases of rigorous clinical trials. Billions ..